This project is an investigation of the role of a vasoactive constituent of blood plasma in the cardiac regulation of coronary blood flow and in the interactions between vascular elements and platelets during aggregation. The plasma factor causes coronary vasoconstriction, improves the cardiac autoregulatory response to changes in perfusion pressure, and inhibits platelet aggregation. This factor also alters the relative amounts of thromboxanes, prostacycline, and other prostaglandins formed from arachidonic acid. The aim of this project is to determine whether or not the physiological effects produced by the plasma factor result from its effects upon prostaglandin and thromboxane synthesis.